Current Issue : October - December Volume : 2014 Issue Number : 4 Articles : 8 Articles
Background: 11 patients were referred to our Molecular Genetics Department at the Royal Devon and Exeter\nHospital between 2000-2012 with a physician�s diagnosis of remitting diabetes. Our aim was to identify patients\nwith remitting diabetes whose clinical presentation is not explained by any known aetiology of diabetes.\nMethods: We obtained longitudinal clinical data on all 11 patients from the hospital records. All patients were\naged between 0.5 and 35 years at diagnosis. We applied clinical criteria derived from the literature to establish\n1) definite diabetes, 2) diabetes initially severe-requiring treatment with insulin, 3) remission of diabetes, and\n4) exclusion of known causes of remitting diabetes.\nResults: 10 out of 11 patients had an alternative explanation for their remission or a clear diagnosis was not\nidentified. We identified a single patient with idiopathic remitting diabetes using these criteria. The patient was a\nwhite Caucasian female diagnosed aged 15 with symptoms of diabetes, laboratory glucose of 21.2 mmol/L and\nHbA1c 134 mmol/mol. Her BMI was 23.6 kg/m2. She was treated with basal bolus insulin but discontinued two\nyears after diagnosis due to hypoglycaemia. 13 years post diagnosis, she had a normal oral glucose tolerance\ntest during pregnancy (fasting glucose 4.5 mmol/L, 2 hr glucose 4.8 mmol/L) and an HbA1c of 30 mmol/mol.\nThis patient does not appear to have Type 1 or Type 2 diabetes, and furthermore does not fit into current\nclassifications of diabetes.\nConclusions: Idiopathic remitting diabetes is rare but does exist. Strict clinical criteria are important to ensure\npatients have a robust clinical diagnosis. Identification of more patients with idiopathic remitting diabetes will\nenable further study of the clinical course of this syndrome. Applying these strict criteria will allow the identification\nof patients with remitting diabetes to assess its aetiology....
Background\nTo compare the first-in-class sodium glucose co-transporter 2 (SGLT2) inhibitor, dapagliflozin, with existing type 2 diabetes mellitus (T2DM) treatment options available within the European Union (EU) for add-on therapy to sulfonylureas (SUs).\n\nMethods\nA systematic review was conducted to identify randomised controlled trials (RCTs) in T2DM patients inadequately controlled by SU monotherapy. Direct meta-analysis, Bucher indirect comparisons and Bayesian network meta-analysis (NMA) were conducted on studies meeting predefined inclusion criteria. Sufficient data were available to assess three clinical endpoints at 24 (+/- 6) weeks follow-up: mean change in HbA1c from baseline, mean change in weight from baseline, and the proportion of patients experiencing at least one episode of hypoglycaemia. The effect of confounding baseline factors was explored through covariate analyses.\n\nResults\nThe search identified 1,901 unique citations, with 1,870 excluded based on title/abstract. From reviewing full-texts of the remaining 31 articles, 5 studies were considered eligible for analysis. All studies were comparable in terms of baseline characteristics, including: HbA1c, age and body mass index (BMI). In addition to dapagliflozin, sufficient data for meta-analysis was available for three dipeptidyl peptidase-4 (DPP-4) inhibitors and one glucagon-like peptide-1 (GLP-1) analogue. Based on fixed-effect NMA, all treatment classes resulted in statistically significant decreases in HbA1c at follow-up compared to placebo. Dapagliflozin treatment resulted in significantly decreased weight at follow-up compared to placebo (-1.54 kg; 95% CrI -2.16, -0.92), in contrast to treatment with GLP-1 analogues (-0.65 kg; 95% CrI -1.37, 0.07) and DPP-4 inhibitors (0.57 kg; 95% CrI 0.09, 1.06). The odds of hypoglycaemia were similar to placebo for dapagliflozin and DPP-4 inhibitor add-on treatment, but significantly greater than placebo for GLP-1 analogue add-on treatment (10.89; 95% CrI 4.24, 38.28). Assessment of NMA model heterogeneity was hindered by the small size of the network.\n\nConclusions\nDapagliflozin, DPP-4 inhibitors and GLP-1 analogues, in combination with SU, all provided better short-term glycaemic control compared to SU monotherapy. Dapagliflozin was the only add-on therapy that had both a favourable weight and hypoglycaemia profile compared to the other classes of treatment evaluated....
Background\nObesity and diabetes mellitus are well-defined risk factors for cardiovascular mortality. The impact of antecedent hyperglycemia and body size on mortality in critical ill patients in intensive care units (ICUs) may vary across their range of values. Therefore, we prospectively analyzed the relationship between in-hospital mortality and preexisting hyperglycemia and body size in critically ill ICU patients to understand how mortality varied among normal, overweight, and obese patients and those with low, intermediate, and high glycated hemoglobin (HbA1c) levels.\n\nMethods\nMedical history, weight, height, physiologic variables, and HbA1c were obtained during the first 24 h for patients who were consecutively admitted to the high complexity ICU of Hospital de ClÃ?Ânicas de Porto Alegre, Brazil, from April to August 2011. The relationships between mortality and obesity and antecedent hyperglycemia were prospectively analyzed by cubic spline analysis and a Cox proportional hazards model.\n\nResults\nThe study comprised 199 patients. The overall hospital mortality rate was 43.2% during a median 16 (8ââ?¬â??28) days of follow-up. There was a progressive risk of in-hospital mortality with higher HbA1c levels, with the relationship becoming significant at HbA1c >9.3% compared with lower levels (hazard ratio 1.74; 95% confidence interval with Bonferroni correction 1.49ââ?¬â??2.80). In contrast, mean body mass index (BMI) was higher in survivors than in nonsurvivors (27.2 kg/m2?Ã?±?7.3 vs. 24.7 kg/m2?Ã?±?5.0 P?=?0.031, respectively). Cubic spline analysis showed that these relationships differed nonlinearly through the spectrum of BMI values. In a Cox proportional hazards model adjusted for Acute Physiology and Chronic Health Evaluation II score and HbA1c, the risk of in-hospital mortality progressively decreased with increasing BMI (BMI <20 vs. 20ââ?¬â??23.9 kg/m2, P?=?0.032; BMI <20 vs. 24ââ?¬â??34.9 kg/m2, P?=?0.010; BMI <20 vs. ?35 kg/m2, P?=?0.032).\n\nConclusions\nOur findings suggest that significant hyperglycemia prior to ICU admission is a risk factor for in-hospital mortality. Conversely, increasing BMI may confer an advantageous effect against mortality in critical illness independently of previous glycemic control....
Background: Quantifying the burden of diabetes mellitus is fundamental for managing patients in health service\ndelivery systems and improves the understanding of the importance of prevention and early intervention of\ndiabetes. In Switzerland, epidemiological data on diabetes are very scarce. In this study we provide a first national\noverview of the current situation of diabetes mellitus in Switzerland as well as the development of the prevalence,\nincidence, mortality and costs between 2006 and 2011.\nMethods: Using health care claims data of a large health insurance group, current epidemiology and costs were\ndetermined from a sample of adult enrollees in 2011. The identification of patients with diabetes was based on\nprescription data of diabetes related drugs using the Anatomical Therapeutic Chemical Classification as proxy for\nclinical diagnosis. We further evaluated changes in epidemiology and costs between 2006 and 2011. All results\nwere weighted with census data to achieve an extrapolation to the Swiss general population level.\nResults: A total of 920�402 patients were enrolled in 2011 and 49�757 (5.4%) were identified as diabetes cases. The\nextrapolated overall prevalence of diabetes in Switzerland was 4.9% (2006, 3.9%). The incidence was 0.58% in 2011\n(2007, 0.63%). The extrapolated mortality rate was 2.6% with no significant change over time. Annual diabetes costs\nto the mandatory health insurance increased from EUR 5,036 per patient in 2006 to EUR 5�331 per patient in 2011.\nConclusions: This study shows a high medical and economic burden of diabetes. The prevalence and costs of\ndiabetes in Switzerland increased substantially over time. Findings stress the need for public health strategies to\nmanage patients with chronic conditions and optimize resource allocation in health service delivery systems....
Background: Hypoglycemic episodes are infrequent in individuals without a history of diabetes mellitus or bariatric\nsurgery. When hypoglycemia does occur in such individuals, an uncommon but important diagnosis to consider is\nnon-islet cell tumor hypoglycemia (NICTH). We report a case of NICTH associated with paraneoplastic insulin-like\ngrowth factor-2 (IGF-2) production and review current relevant medical literature.\nCase presentation: A 60 year old male with no relevant past medical history was referred to the endocrinology\nclinic with 18 month history of episodic hypoglycemic symptoms and, on one occasion was noted to have a\nfingerstick glucose of 36 mg/dL while having symptoms of hypoglycemia. Basic laboratory evaluation was\nunrevealing. Further evaluation however showed an elevated serum IGF-2 level at 2215 ng/mL (reference range\n411ââ?¬â??1248 ng/mL). Imaging demonstrated a large right suprarenal mass. A right nephrectomy with resection of the\nmass demonstrated a malignant solitary fibrous tumor. Post resection, the patientââ?¬â?¢s IGF-2 levels normalized and\nhypoglycemic symptoms resolved.\nConclusion: Due to the structural and biochemical homology between IGF-2 and insulin, elevated levels of IGF-2\ncan result in hypoglycemia. A posttranslational precursor to IGF-2 known as ââ?¬Å?big IGFââ?¬Â also possesses biologic activity.\nReview of recent reported cases of NICTH identified widespread anatomic locations and varied pathologic diagnoses of\ntumors associated with paraneoplastic production of IGF-2 causing hypoglycemia. Definitive management of\nhypoglycemia associated with paraneoplastic production of IGF-2 consists of resection of the tumor responsible\nfor IGF-2 production. Accumulating literature provides a firm basis for routine IGF-2 laboratory evaluation in\npatients presenting with spontaneous hypoglycemia with no readily apparent cause....
Background: Previously considered as a disease of the affluent, west or urban people and not of public health\nimportance, diabetes mellitus is increasingly becoming a significant cause of morbidity and mortality in sub-Saharan\nAfrica. However, population-based data to inform prevention, treatment and control are lacking.\nMethods: Using the WHO STEPwise approach to chronic disease risk factor surveillance, a population-based,\nnationwide cross-sectional survey was conducted between July and September 2009 on participants aged 25ââ?¬â??64\nyears. A multi-stage cluster sample design and weighting were used to produce a national representative data for\nthat age range. Detailed findings on the magnitude of diabetes mellitus and impaired fasting blood glucose are\npresented in this paper.\nResults: Fasting blood glucose measurement was conducted on 3056 participants (70.2% females, 87.9% from rural\nareas). The age- sex standardised population-based mean fasting blood glucose was 4.3 mmol/L (95% CI 4.1-4.4 mmol/L)\nwith no significant differences by age, sex and location (urban/rural). The overall prevalence of impaired fasting\nblood glucose was 4.2% (95% CI 3.0%-5.4%). Prevalence of impaired blood glucose was higher in men than in\nwomen, 5.7% (95% CI 3.9%-7.5%) vs 2.7% (95% CI 1.6%- 3.8%), p < 0.01. In both men and women, prevalence of\nraised fasting blood glucose or currently on medication for diabetes was 5.6% (95% CI 2.6%- 8.5%). Although the\nprevalence of diabetes was higher in men than women, 6.5% (95% CI 2.6%-10.3%) vs 4.7% (95% CI 2.4%-7.0%), in\nrural than urban, 5.4% (95% CI 2.4%-8.4%) vs 4.4% (95% CI 2.8%-5.9%) and in males in rural than males in urban,\n6.9% (95% CI 2.8%-11.0%) vs 3.2% (95% CI 0.1%-6.3%), the differences were not statistically significant, p > 0.05.\nCompared to previous estimates, prevalence of diabetes increased from <1.0% in 1960s to 5.6% in 2009 (this study).\nConclusion: High prevalence of impaired fasting blood glucose and diabetes mellitus call for the implementation of\nprimary healthcare approaches such as the WHO package for essential non-communicable diseases to promote healthy\nlifestyles, early detection, treatment and control....
Background: Testicular morphology and immunohistochemical studies have never been reported in genetically\ndocumented adult patients with 5 alpha-reductase type 2 deficiency (5?-R2 deficiency).\nCase presentation: We describe the testicular histopathology of a 17-year-old XY subject with 5?-R2 deficiency\ncaused by the recurrent homozygous Gly115Asp loss of function mutation of the SRD5A2 gene.We also performed\nan immunohistochemical analysis in order to further study the relationship between seminiferous tubules structure,\nSertoli cell differentiation and androgenic signaling impairment in this case. We thus evaluated the testicular\nexpression of the anti-M�¼llerian hormone (AMH), androgen receptor (AR) and 3?-hydroxysteroid dehydrogenase\n(3?HSD). Histological analysis revealed a heterogeneous aspect with a majority (92%) of seminiferous tubules (ST)\npresenting a mature aspect but containing only Sertoli cells and devoid of germ cells and spermatogenesis. Focal\nareas of immature ST (8%) were also found. Testicular AR and 3?HSD expression were detected in adult male\ncontrol, 5?-R2 deficiency and CAIS subjects. However, AMH expression was heterogeneous (detectable only in\nfew AR negative prepubertal ST, but otherwise repressed) in the 5?-R2 deficiency, conversely to normal adult testis\nin which AMH was uniformly repressed and to an adult CAIS testis in which AMH was uniformly and strongly\nexpressed.\nConclusion: Intratesticular testosterone can repress AMH by itself, independently of its metabolism into\ndihydrotestosterone. We also compare our results to the few post pubertal cases of 5?-R2 deficiency with available\nhistological testicular description, reported in the literature. We will discuss these histological findings, in the\nmore general context of evaluating the fertility potential of these patients if they were raised as males and were\nazoospermic....
Background: Obesity and gestational diabetes (GDM) in pregnancy are recognized risk factors for adverse outcomes,\nincluding cesarean section (CS), macrosomia and preeclampsia. The aim of this study was to investigate the\nindependent effect of GDM and obesity on the adverse pregnancy outcomes at term.\nMethods: A retrospective cohort of postpartum women, in King Khalid University Hospital, were stratified according to\nbody mass index (obese ?30 kg/m2, non-obese <30 kg/m2) and the results of GDM screening into the following\ngroups, women with no obesity and no GDM (reference group), women with no obesity but with GDM, women\nwith obesity but no GDM and women with both GDM and obesity. Adverse pregnancy outcomes included high\nbirth weight, macrosomia, CS delivery and preeclampsia. Multiple logistic regression used to examine independent\nassociations of GDM and obesity with macrosomia and CS.\nResults: 2701 women were included, 44% of them were obese and 15% had GDM. 63% of the women with GDM\nwere obese. There was significant increase in the percentage of macrosomia, P < 0.001, high birth weight, P < 0.001, CS,\nP < 0.001 and preeclampsia, P < 0.001 in women with GDM and obesity compared to the reference group. Obesity\nincreased the estimated risk of CS delivery, odds ratio (OR) 2.16, confidence intervals (CI) 1.74-2.67. The combination\nof GDM and obesity increased the risk of macrosomia OR 3.45, CI 2.05-5.81 and the risk of CS delivery OR 2.26,\nCI 1.65-3.11.\nConclusion: Maternal obesity and GDM were independently associated with adverse pregnancy outcomes. The\ncombination of both conditions further increase the risk....
Loading....